27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Florbetapir PET can be used to detect increased cerebral-to-cerebellar fibrillar Aβ burden in a Down syndrome patient with Alzheimer disease, even in the presence of frequent amyloid angiopathy and diffuse plaques in the cerebellum. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Down syndrome (DS) is a common genetic condition caused by the presence of three copies of chromosome 21 (trisomy 21). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Down syndrome (DS), oxidative DNA-damage may play a role in the pathogenesis of characteristic mental retardation and precocious dementia of Alzheimer type. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The human amyloid beta protein is the major constituent of the brain amyloid plaques found in Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In adults with DS, early amyloid-β accumulation in the striatum is divergent from sporadic AD; however, despite the early striatal amyloid-β, glucose hypometabolism was confined to the typical AD-associated regions, which occurs similarly in autosomal dominant AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
People with Down syndrome (DS) have increased risk of Alzheimer disease (AD), presumably conferred through genetic predispositions arising from trisomy 21. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To identify changes in brain functions associated with the development of dementia, brain metabolism and cognition were assessed repeatedly in 12 adults with Down syndrome (DS) using positron emission tomography and neuropsychological tests. 3 key findings →
Participants: 12 Evidence: low
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We propose that sleep disruption is a lever arm that influences how cognition emerges in development and then declines in response to Alzheimer disease in people with Down syndrome. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This review describes recent discoveries in neurobiology of Down syndrome (DS) achieved with use of mouse genetic models and provides an overview of experimental approaches aimed at development of pharmacological restoration of cognitive function in people with this developmental disorder. 1 key finding →
Evidence: low
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Dementia of the Alzheimer type (DAT) is common in older persons with Down syndrome (DS). 1 key finding →
Participants: 55 Evidence: low
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In vivo MRI biomarkers can support the diagnosis of early-onset cerebral amyloid angiopathy, which might already be present in pediatric Down syndrome patients. 2 key findings →
Participants: 12 Evidence: low
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The findings of this study highlight the importance of accurate mortality data for studying and addressing population health trends. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundLifetime incidence of Alzheimer's disease (AD) in Down syndrome (DS) exceeds 90%. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with DS may have unique neuro- and cardio- protective factors that deserve future investigation. 4 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with DS are often supported by family caregiver(s), who face challenges including lack of awareness of the increased risk of developing AD, difficulty in obtaining a timely diagnosis, limited resources for psychosocial support, and lack of access to clinical trials. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
To study the use of a dementia screening tool in our clinic cohort of adults with Down syndrome. 1 key finding →
Participants: 14 Evidence: moderate
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The objective of this study was to use high-resolution MRI techniques to determine whether children with Down syndrome exhibit decreases in hippocampal and amygdala volumes similar to those demonstrated in recent studies of adults with this condition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ts65Dn mouse displays a partial triplication of chromosome 16 and is adopted as a model for Down syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is one of the commonest disorders with huge medical and social cost. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia are critical in brain development and Alzheimer's disease (AD) etiology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is one of the leading causes of intellectual disability, and patients with DS face various health issues, including learning and memory deficits, congenital heart disease, Alzheimer's disease (AD), leukemia, and cancer, leading to huge medical and social costs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is associated with a number of deleterious phenotypes, including learning disability, heart defects, early-onset Alzheimer's disease and childhood leukaemia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this article, we first present a summary of the general assumptions about Down syndrome (DS) still to be found in the literature. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta protein (Abeta) deposition was investigated in the frontal cortex of 8 cases of (genetically confirmed) chromosome 14-linked Alzheimer's disease (AD) using the end-specific monoclonal antibodies BA27 and BC05 to detect the presence of Abeta40 and Abeta42(43), respectively. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain derived neurotrophic factor (BDNF) and its receptor tropomyosin-related kinase B (TrkB) play crucial roles in neuronal development, synaptic transmission, and neuroplasticity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 534 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →